We are characterizing the biological functions and biochemical constitution of new membrane antigens on malaria-infected erythrocytes to ascertain their roles in parasite evasion of host immunity. Plasmodium falciparum-infected erythrocytes express antigenic knobs on their surface which mediate attachment to venular endothelium. Sequestration of infected cells from the peripheral circulation prevents their passage through the spleen. Localized spleen-dependent immune responses are thereby avoided. An in vitro assay for attachment to endothelial cells and melanoma cells has been developed allowing us to explore ways to block attachment. Plasmodium knowlesi infected erythrocytes express a surface variant antigen which changes during chronic infection. We have shown that variant antigen is involved not only in evasion of variant-specific immunity, but also in suppression of other spleen-dependent parasiticidal immune responses. Variant antigen expression per se, and the parasites capacity to alter variant antigen are both dependent on the presence of ths host spleen. The variant antigen has also been identified as a membrane protein synthesized by the introarythrocytic malaria parasite.